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House dust mite allergen Der p 1 effects on sinonasal epithelial tight junctions
Author(s) -
Henriquez Oswaldo A.,
Beste Kyle Den,
Hoddeson Elizabeth K.,
Parkos Charles A.,
Nusrat Asma,
Wise Sarah K.
Publication year - 2013
Publication title -
international forum of allergy and rhinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.503
H-Index - 46
eISSN - 2042-6984
pISSN - 2042-6976
DOI - 10.1002/alr.21168
Subject(s) - tight junction , antigen , epithelium , immunofluorescence , antibody , microbiology and biotechnology , medicine , immunology , biology , pathology
Background Epithelial permeability is highly dependent upon the integrity of tight junctions, which are cell‐cell adhesion complexes located at the apical aspect of the lateral membrane of polarized epithelial cells. We hypothesize that sinonasal epithelial exposure to Der p 1 house dust mite antigen decreases expression of tight junction proteins (TJPs), representing a potential mechanism for increased permeability and presentation of antigens across the sinonasal epithelial layer. Methods Confluent cultured primary human sinonasal epithelial cells were exposed to recombinant Der p 1 antigen vs control, and transepithelial resistance measurements were performed over 24 hours. Antibody staining for a panel of TJPs was examined with immunofluorescence/confocal microscopy and Western blotting. Tissue for these experiments was obtained from 4 patients total. Results Der p 1 exposed sinonasal cells showed a marked decrease in transepithelial resistance when compared to control cells. In addition, results of Western immunoblot and immunofluorescent labeling demonstrated decreased expression of TJPs claudin‐1 and junction adhesion molecule‐A (JAM‐A) in Der p 1–exposed cultured sinonasal cells vs controls. Conclusion Der p 1 antigen exposure decreases sinonasal epithelium TJP expression, most notably seen in JAM‐A and claudin‐1 in these preliminary experiments. This decreased TJP expression likely contributes to increased epithelial permeability and represents a potential mechanism for transepithelial antigen exposure in allergic rhinitis.